Excessive levels of certain saturated fatty acids cause
mitochondria to fragment, leading to insulin resistance in skeletal muscle, a
precursor of type 2 diabetes, according to a paper in the January issue of the
journal Molecular and Cellular Biology.
This is the first time mitochondrial fragmentation has been implicated in
insulin resistance, says corresponding author Yau-Sheng Tsai, of the College of
Medicine, National Cheng Kung University, Taiwan, Republic of China.

Mitochondria are the intracellular machines that turn sugar
into energy, and skeletal muscle is packed with them. Normally, cells respond
to insulin, a hormone, by importing glucose from the bloodstream. Type 2
diabetes is characterized by insulin resistance, a cellular impairment in
glucose uptake.

The new research offers an explanation for this phenomenon.
“Disruption of mitochondrial dynamics may underlie the pathogenesis of muscle
insulin resistance in obesity and type 2 diabetes,” says Tsai. That explanation
suggests a hypothetical treatment. “Manipulating mitochondrial morphology may
provide a novel therapeutic strategy for insulin resistance and type 2
diabetes,” says Tsai. In the study, the research showed that inhibiting
mitochondrial fission in mouse models reduced the insulin resistance, he says.

The study also supports previous research suggesting that
reducing saturated fats in the diet would reduce insulin resistance, says Tsai.
“It has been well documented that saturated fatty acids can lead to insulin
resistance in humans and rodents.” Palmitate, a particularly harmful saturated
fatty acid, “is very abundant in lard, butter, and margarine,” says Tsai.

“Most studies of mitochondria and diabetes have focused on
mitochondrial quantity, and they all
agree that increasing mitochondrial biogenesis does help mitochondrial function
and cellular metabolism,” says Tsai. “Our study showed that maintaining the
balance of mitochondrial dynamics is
also important for mitochondria to maintain normal function.”